An Update on the Chemokine System in the Development of NAFLD

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. Sustained hepatic inflammation is a key driver of the transition from simple fatty liver to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. Hepatic inflammation is orchestrated by...

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Published inMedicina (Kaunas, Lithuania) Vol. 58; no. 6; p. 761
Main Authors Nagata, Naoto, Chen, Guanliang, Xu, Liang, Ando, Hitoshi
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 05.06.2022
MDPI
Subjects
Bone marrow
chemokine
Chemokines
Diet
Hepatitis
immune cells
Immune system
Inflammation
Insulin resistance
Kinases
Ligands
Liver
Lymphocytes
Neutrophils
nonalcoholic fatty liver disease
nonalcoholic steatohepatitis
Pathogenesis
Proteins
Review
Small intestine
Tumor necrosis factor-TNF
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Summary:Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. Sustained hepatic inflammation is a key driver of the transition from simple fatty liver to nonalcoholic steatohepatitis (NASH), the more aggressive form of NAFLD. Hepatic inflammation is orchestrated by chemokines, a family of chemoattractant cytokines that are produced by hepatocytes, Kupffer cells (liver resident macrophages), hepatic stellate cells, endothelial cells, and vascular smooth muscle cells. Over the last three decades, accumulating evidence from both clinical and experimental investigations demonstrated that chemokines and their receptors are increased in the livers of NAFLD patients and that CC chemokine ligand (CCL) 2 and CCL5 in particular play a pivotal role in inducing insulin resistance, steatosis, inflammation, and fibrosis in liver disease. Cenicriviroc (CVC), a dual antagonist of these chemokines’ receptors, CCR2 and CCR5, has been tested in clinical trials in patients with NASH-associated liver fibrosis. Additionally, recent studies revealed that other chemokines, such as CCL3, CCL25, CX3C chemokine ligand 1 (CX3CL1), CXC chemokine ligand 1 (CXCL1), and CXCL16, can also contribute to the pathogenesis of NAFLD. Here, we review recent updates on the roles of chemokines in the development of NAFLD and their blockade as a potential therapeutic approach.
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These authors contributed equally to this work.
ISSN:1648-9144
1010-660X
1648-9144
DOI:10.3390/medicina58060761